Abstract
Rheumatoid Arthritis and Type One Diabetes are devastating clinical conditions characterized by the Autoantibody production against self, affecting up to 5% of population which, ultimately leads to a destruction of cartilage, bones and, insulin; producing Beta cells of Pancreas. As both environmental and genetic factors contribute to these conditions (50-60%). The focus of our review is to enlist that either combined evidence shows the association of Protein Tyrosine Phosphatase Non-receptor type 22 C1858T Polymorphism with these two devastating conditions are not. A minor but most prominent allele of Protein Tyrosine Phosphatase Non-receptor type 22 gene, W620, plays a crucial role in the disease initiation process. The web sources we use for data collection were Google Scholar, PubMed, Online Mendelian Inheritance in Man, and Science Direct. At the same time, the Mesh term of our search was the role of Protein Tyrosine Phosphatase Non-receptor type 22 gene, Single Nucleotide Polymorphism C1858T, 620W, Arg620Trp in Rheumatoid Arthritis and Type One Diabetes. The data set was consist of 210 research articles, which reviewed critically; 73 highly related articles were selected for data extraction to give knowledge to the reader at a glance. Also, taking into account the futuristic perspective for researchers that need further evaluation and will ultimately lead to drug development that will aid enhancement in therapeutics.
Highlights
Almost every disease has some genetic background as well as some unique features upon which the future research methods are designed
Reproducibility was checked by conduction of another study was conducted from the Czech population southeast but had slight differences [44]. They have included 396 patients and genotype the single nucleotide polymorphism occurs in them (SNP) with in the gene PTPN22 at position C1858T beside this 1178 matched controls with no history of T1D was taken from north central Florid, they include causcasian families from Human Biological Data interchange the patients was diagnosed according to the criteria of national Diabetes Data Group. clinical information of the patient is present in [45,46,47]
The major role in autoimmune diseases is played by the minor allele W620 which results due to SNP at position 1858 causes the substitution of C=>T (C1858T) and is confirmed by the accumulation of the higher amount of T allele in samples as mention in both of above studies
Summary
Almost every disease has some genetic background as well as some unique features upon which the future research methods are designed. The advancement in molecular genetics and the development of hight throughput methods for investigation of causing factors of diseases have led to the identification of several genes and loci in both Rheumatoid Arthritis and T1D. Some of these genes are disease-specific like CD2/CD58, TNFAIP3, PRDM1, BLK involved in Rheumatoid Arthritis but is not responsible for T1D. There are a lot of genes that is not connected with the MHC complex These genes play an essential role in the susceptibility of an individual to exposer to autoimmune diseases, like cytoplasmic protein tyrosine phosphatase Non-receptor type 22 ( PTPN22) gene. The main focus of the review article is the role of PTPN22 in autoimmune diseases and how its allele act as susceptibility agent for individual toward Rheumatoid Arthritis and T1D
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